Three main types of prosopagnosia are distinguished in literature: acquired, developmental and congenital. Acquired prosopagnosia appears after a clearly identifiable event; head trauma, stroke or other damage to the occipito-temporal brain areas (e.g. Schiltz et al, 2006). In most literary cases though, some other visual deficits are apparent (e.g. J.J. Barton, Cherkasova, Press, Intriligator & Connor, 2003), or there are problems with recognition of not just faces, but other visual categories as well (e.g. De Haan & Campbell, 1991). This is caused by the diverse nature of the injured area, and also by the small size of brain areas reasonable for face recognition, and their connection and proximity to brain areas responsible for different functions.

Chronologically, the acquired disorder appeared first in literature, since the two world wars resulted in many brain injured people. One of the first reports examined the case of three soldiers injured in the II. World War. Their brain injuries resulted in different severity of face recognition and other visual problems (e.g. object recognition disorder), depending on the expanse of their injuries (Bodamer, 1947).

An other type of the disorder is the so called developmental prosopagnosia; this expression is an umbrella term that does not tell anything about the origin of the disorder (Grueter et al, 2007).

In developmental cases, there is no documented brain damage, intelligence is usually within the normal range, and no lower level visual impairment is apparent (e.g. Rivolta, Schmalzl, Coltheart & Palermo, 2010). There is no undoubting evidence however, that the symptoms could not be connected to perinatal complications (e.g. oxygen-deprived condition), which could remain hidden in case history (Kennerknecht et al, 2006).

In cases where the above mentioned brain damages and perinatal complications can be ruled out, but the person still has difficulties with recognising familiar faces, we may have a case of congenital prosopagnosia (e.g. Stollhoff, Jost, Elze & Kennerknecht, 2010). In these cases it can be determined with high certainty – mostly through parental reports – that the impairment has been present from early childhood and the emergence of the problem can not be connected to any brain malformation. It is known that infants take an interest in stimuli resembling facial configurations almost immediately after birth (Morton & Johson, 1991), therefore it is thought that this innate face preference might be impaired in congenital prosopagnosia. Considering the fact that the impairment is observed from birth, a role of hereditary factors can not be excluded in these cases (de Gelder & Stekelenburg, 2005). However, in the absence of a genetic test, using the term hereditary prosopagnosia is only correct if there are blood relatives who also suffer from a face recognition disorder (although this term is often used as a synonym for the congenital form) (Kennerknecht et al, 2006).

There have only been few studies examining the genetic background of the disorder, therefore we can only draw inferences on the heredity through anecdotal reports of prosopagnosic patterns appearing in a family through generations.